4.5 Article

Taste sensitivity to 6-n-propylthiouracil is associated with endocannabinoid plasma levels in normal-weight individuals

Journal

NUTRITION
Volume 29, Issue 3, Pages 531-536

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.nut.2012.09.018

Keywords

6-n-Propylthiouracil taste sensitivity; Control of eating behavior; Endocannabinoids; Oleoylethanolamide; Normal-weight subjects

Funding

  1. Italian Ministry of University and Research
  2. Fondazione Banco di Sardegna

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Objective: A decreased sensitivity to 6-n-propylthiouracil (PROP) has been shown to be associated with increased energy intake and therefore an increased body mass index, although other studies have not confirmed this association, suggesting the involvement of other factors. We investigated whether the endocannabinoid system, which also modulates hunger/satiety and energy balance, plays a role in modulating eating behavior influenced by a sensitivity to PROP. Methods: The plasma profile of the endocannabinoids 2-arachidonoylglycerol (2-AG), anandamide (AEA), and congeners of AEA, palmitoylethanolamide and oleylethanolamide (OEA), was determined in normal-weight PROP supertasters (STs) and PROP non-tasters (NTs). A cognitive eating behavior disorder was assessed by the Three-Factor Eating Questionnaire, which estimates dietary restraint, disinhibition, and perceived hunger. Results: The disinhibition score of NTs was higher than those of STs (P = 0.02). Moreover, in NTs, OEA was inversely correlated to the perceived hunger score (r = -0.7, P = 0.002), and AEA was positively correlated to the restraint score (r = 0.5, P = 0.04) and negatively to the perceived hunger score, although the latter correlation was at the limit of statistical significance (r = -0.47, P = 0.05). In addition, we found lower concentrations of AEA and 2-AG in the plasma of NT compared with ST subjects (AEA, P = 0.034; 2-AG, P = 0.003). Conclusions: Our data suggest that a higher disinhibition behavior in NTs may be compensated in part, in normal-weight subjects, by the decrease of peripheral endocannabinoids to downregulate the hunger-energy intake circuitry. (C) 2013 Elsevier Inc. All rights reserved.

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